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Hannah R. Joo, Shih-Kuo Chen, Beth Peterson, Dennis M. Dacey, Samer Hattar; Intraretinal Axon Collaterals of Melanopsin Cells in Primate and Mouse Terminated in the Inner Plexiform Layer. Invest. Ophthalmol. Vis. Sci. 2012;53(14):4345.
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© ARVO (1962-2015); The Authors (2016-present)
The axons of retinal ganglion cells are unique in that they typically do not provide synaptic feedback to the retina via recurrent axon collaterals. Such collaterals, however, have been consistently observed in many species, including primate. The ganglion cells giving rise to these collaterals have large, sparsely branching dendritic trees, suggesting the collaterals are not a developmental aberration but are associated with a single, low-density ganglion cell population.
Using a transgenic mouse (Opn4CreERT2; Z/AP) in which the density of labeled melanopsin cells is controlled by tamoxifen injection, we are able to sparsely label ipRGCs and unambiguously trace their dendritic structure and axon.
Here we show that, in both mouse and primate, these intraretinal collaterals arise from a subset of melanopsin-expressing cells. In mouse, intraretinal axon collaterals that terminate either inner or outer and can be clearly traced to individual M1 or M3 cells (~8% total). In macaque retina, a subpopulation (~11%) of giant melanopsin immunoreactive cells also exhibit axon collaterals, indicating that the primate giant axon collateral-bearing cells are melanopsin cells.
The intraretinal collaterals of ipRGCs suggest a critical role for this novel feedback pathway in retinal circadian rhythms. Further anatomical and physiological analysis is required to elucidate the role of these cells in signaling irradiance to the retina, possibly via the dopaminergic amacrine system.
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